Anaesthesiology Intensive Therapy, 2011,XLIII,3; 150-151

Severe Pneumocystis jiroveci infection in an immunocompromised patient after splenectomy

*Krzysztof Tracz1, Anna Kuczewska2, Jacek Kulesza1

1Department of Anaesthesiology and Intensive Therapy, 1st Municipal Hospital in Gdynia

2NZOZ u Źródła Marii w Gdyni

Background. Pneumocystis jiroveci (old name Pneumocystis carini) can cause severe pneumonia in immunecompromised patients, most commonly those who are HIV infected.

Case report. A 68-yr-old man, who eight years earlier had undergone trauma related splenectomy, was admitted to ITU after a cardiac arrest due to septic shock caused by an unknown pathogen. He had been treated for three weeks with various antibiotics without improvement. On the second day after resuscitation, high concentration of IgM anti-Pneumocystis jivecii antibodies was found, and high-dose trimetoprim therapy was started and continued for two weeks. Further treatment was complicated by ventilator-associated pneumonia (Acinetobacter baumannii); the patient eventually recovered without any neurological sequelae, and was transferred to a low-dependency area after 4 weeks in ITU. 

Conclusion. We conclude that Pneumocystis jiroveci infection should be suspected as a cause of severe pneumonia in splenectomised patients.

Pneumocystis jiroveci pneumonia (PJP) is caused by a fungus Archiascomycetes, initially classified as a protozoon and later called Pneumocystis carinii. In 1999, Frankel [1] suggested the presently used name, officially accepted in 2001 [2]. In immunocompromised individuals (HIV), Pneumocystis jiroveci causes severe interstitial pneumonia.

The objective of the present report was to describe the diagnostic procedure and treatment of a patient with Pneumocystis jiroveci pneumonia. 


A 67-year-old male patient was admitted to the medical ward due to dyspnoea at rest, cough, chest oppression and joint pain. For a month, he had been treated for pneumonia by the general practitioner. On admission, his general condition was quite good, temperature up to 38º C. Eight years earlier, he had undergone splenectomy due to trauma. The slight interstitial densities detected radiologically on admission progressed during hospitalization resulting in massive fuse interstitial consolidations in both lungs. Despite the use of many antibiotics (amoxicillin with clavulanic acid, ceftazidime, azithromycin, sulfamethoxazole with trimethoprim, piperacillin with tazobactam, netilmicin), his condition deteriorated with the temperature rising to 39º C. The CRP concentration increased from 8.2 mg dL-1 to 23.2 mg dL-1 whereas WBC from 14.19 G L-1 to 19.74 G L-1. The total lymphocyte count, on the other hand, decreased from 3.5 G L-1 to 2.4 G L-1. The concentration of procalcitonin on admission was 2.55 ng mL-1 and
of LDH 574 U L-1.

During the 3-week hospitalization, repeated cultures of blood, urine, and bronchial tree secretion were negative. There were no IgM antibodies against Chlamydia pneumoniae, Mycoplasma pneumoniae and Borrelia detected in serum; the urine analysis for the Legionella pneumofilae antigen was negative. The CT scan of the lungs demonstrated diffuse foci of densities, despite the fact that in lung biopsy specimens collected during bronchofibrescopy no lesions were found. On day 19, the patient developed cardiac arrest and after successful resuscitation was transferred to the ITU. On admission to ITU, he was unconscious (GCS 3). Severe sepsis was diagnosed (PaO2/FIO2 195, creatinine 206.8 µmol L-1, BE – 9.9 mEq L-1; WBC 23.4 G L-1, body temperature 38.7º C. Increased values of PaO2/FIO2 were recorded for another two weeks of hospitalisation. Artificial lung ventilation was initiated and continued for 25 days (max. values of FIO2 0.6; PEEP+8 cm H2O/0,8 kPa). The cardiovascular system was supported with intravenous infusion of noradrenaline in the dose of 0.5 µg kg-1min-1.

On ITU day 2, high concentration of IgM anti-Pneumocystis jiroveci antibodies was found. Trimethoprim with sulfamethoxazole was instituted in the daily dose of 12 mg kg-1, which was discontinued after 15 days due to a decrease in thrombocyte count from  424 G L-1 to 78.7 G L-1 on day 10 and further to 12.4 G L-1 on day 15. Five units of PLT were administered.

The therapy was complicated with ventilator-associated pneumonia (Acinetobacter baumani) and urinary infection (Enterococus faecalis). The targeted antibiotic therapy was initiated, which proved effective as WBC decreased from 23.4 G L-1 to 7.0 G L-1 (day 19) and CRP from 28.3 mg dL-1 to 5.5 mg dL-1. After 24 days of ITU therapy, the patient regained consciousness and several days later was transferred to the medical ward for further treatment.


The case described demonstrates the difficulties encountered while searching for the pneumonia-inducing factor in a patient with the history of splenectomy. The long-term and inefficient empiric therapy of the disease resulted in severe respiratory failure and ultimately led to cardiac arrest. Many studies addressed Pneumocystis pneumonia in immunocompromised patients [1, 2, 3, 4, 5]. This kind of infection is common yet its pathogenicity is strictly associated with the immune condition of patients. In those with normal immune functions, the infection is usually asymptomatic while in immunocompromised individuals, the infection can cause interstitial pneumonia, which is likely to lead to death (e.g. in AIDS patients). The infection-related mortality, even in individuals not infected with HIV, is high reaching 50% [2].

In our case, after two months of failed treatment, the patient developed severe sepsis resulting in cardiac arrest. It appears that severe course of the disease resulted from the impaired immune function due to splenectomy performed many years earlier. Pneumocystis pneumonia was difficult to diagnose, as it did not differ from the typical pneumonia. The patient complained of dyspnoea at rest, dry cough, thoracic discomfort, weight loss and shivers. Moreover, the X-ray-detected inflammatory changes were not characteristic of this infection. They were fuse interstitial densities; and the typical PJP X-ray showed hilar infiltrations. A sensitive marker (sensitivity 70-100%) of Pneumocystis infection, based on which the extent of lung damage can be determined, is the concentration of LDH, which in our case was elevated. Pneumocystis jiroveci infections affect not only lungs but also other organs, e.g. the CNS, bone marrow (pancytopenia), lymph nodes, eyes (retinal lesions), thyroid, and gastrointestinal system.

The case presented shows how dramatic Pneumocystis jiroveci infection can be in patients after splenectomy. Furthermore, it proves that in infections with high death risk, proper diagnosis and suitable therapeutic procedures markedly improve the prognosis.



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5.     Gerrard JG: Pneumocystis carinii pneumonia in HIV-negative immunocompromised adults. Med J Aust 1995; 162: 223.

6.     Saksasithon S, Sungkanuparph S & Thanakitcharu S: Pneumocystis carinii pneumonia in patients without HIV infection. J Med Assoc Thai 2003; 86: 612-616.

7.     Sepkowitz KA: Opportunistic infections in patients with and patients without acquired immunodeficiency syndrome. Clin Infect Dis 2002; 34: 1098-1107.



*Krzysztof Tracz

Oddział Anestezjologii i Intensywnej Terapii
I Szpital Miejski w Gdyni
ul. Wójta Radtkego 1, 81-348 Gdynia

received: 17.03.2011
accepted: 22.07.2011